Several key growth factors and hormones control muscle development. Of these, testosterone and insulin-like growth factor 1 (IGF-1) are extremely important.

Testosterone & IGF-1 Stimulate Muscle Growth

Testosterone is a steroid hormone that triggers the reading of genes coding for proteins essential for muscle development. By mechanistic contrast, IGF-1 promotes the physical elaboration of these proteins once their genes have been read. Hence, the participation of both these myogenic (muscle generating) agents is needed for optimal muscle development.

LH & GH Mobilize Testosterone & IGF-1, Respectively

Upstream of muscle, two hormones are responsible for activating testosterone and IGF-1 expression. Luteinizing hormone (LH) released from the anterior pituitary (a gland located at the base of our brains) causes the testicles of a male to produce testosterone, which is then released into the blood stream for broad distribution to the body’s musculature. On the other hand, Growth hormone (GH) also released from the anterior pituitary causes the liver to produce IGF-1 similarly for systemic distribution.

LH & GH Release Are Induced by Exercise

Both LH (testosterone releaser) and GH (IGF-1 releaser) are anabolic with reference to skeletal muscle, since they ultimately increase the production of proteins needed for muscle maturation. Moreover, exercise further augments the release of LH and GH from the anterior pituitary. This combination of effects explains why testosterone and IGF-1 play a critical role in muscle growth in response to training. Importantly, this metabolic scenario is short circuited in the elderly.

Revising the IGF-1 Dogma

It was once thought that the only way to produce IGF-1 was in response to growth hormone released from the anterior pituitary gland. This dogma needs to be revised, however, since it has now known that skeletal muscle can produce its own allotment of IGF-1 (for local, not systemic, use) in response to appropriate stimuli. One such stimulus that incites muscle cells to directly produce IGF-1 is exercise. Another surprising stimulus that causes muscle to produce IGF-1 will be discussed shortly…

Exercise Also Stimulates IGF-1 Production

Exercise thus provokes the release GH from the anterior pituitary, which then stimulates the liver to produce IGF-1 for long-range action. Exercise, however, also causes muscle cells to produce their own IGF-1 for local (purely muscular) use.

Learn what environmental factors (exercise, nutrition, etc…) influence the release GH (and hence, IGF-1…) at the following link: http://www.creatinemonohydrate.net/growth_hormone.html

New Research: Creatine Directly Stimulates IGF-1 Production

Recent scientific research has now shown that creatine also stimulates skeletal muscle cells to produce IGF-1 in the absence of GH. More importantly, creatine exerts this effect independently of exercise as well. That is, simply raising muscle cells in plastic dishes (and hence, away from the central nervous commands to move) and adding creatine to their surrounding environment, causes them to produce IGF-1; again, without the participation of GH. This IGF-1 is then released locally to stimulate neighboring muscle cells into forming force-generating muscle fibers.

It thus appears that creatine alone, without the assistance of GH or exercise, is able to stimulate muscle cells to produce IGF-1. The implications of this finding are enormous… Concisely, individuals that are restricted in movement due to injury or disease might benefit from creatine supplementation as a result of its ability to help retain muscle mass.

How creatine stimulates muscular IGF-1 production is explained at the following link: http://www.creatinemonohydrate.net/creatine_sarcopenia.html

Muscular Dystrophy

Reduced levels of IGF-1 also characterize certain forms of Muscular Dystrophy, raising the intriguing possibility that creatine supplementation may be then used as an adjuvant treatment for these disorders. This possibility has not escaped the attention of scientific funding agencies as is described in the following link and will be the topic of a future post.

Learn how creatine supplementation might be used to combat the debilitating symptoms of Muscular Dystrophy and other neuromuscular disorders at the following link: http://www.creatinemonohydrate.net/creatine_trials.html

Sarcopenia

As eluded to earlier, the major cause of muscle loss in the elderly (a clinical condition known as sarcopenia) is a decline in IGF-1 and testosterone with advanced age. Creatine supplementation may then be a way to partially offset muscle loss in the elderly. In a sense, creatine supplementation may help keep us young…

Learn how creatine supplementation might help counteract the characteristic loss of muscle mass in the elderly at the following link: http://www.creatinemonohydrate.net/creatine_sarcopenia.html

Immobilization Atrophy

Immobilizing a limb (as when placed in a cast) also causes a form of muscle loss, a process known as disuse atrophy. Importantly, creatine supplementation has also been shown to alleviate some of the muscle damage caused by limb immobilization. This will be covered in a subsequent post. Stay tuned…

To conclude, it was once thought that creatine’s only benefit was to increase energy availability during strenuous exercise. It is now becoming clear, however, that creatine possesses other provocative (previously hidden) benefits that will have even greater ramifications for muscle development; the ability to locally produce IGF-1 is just one…

More background to this post can be found in my creatine guide: http://www.creatinemonohydrate.net/creatine_guide.html

Is creatine too good to be true? Read about its validated side effects at the following link: http://www.creatinemonohydrate.net/creatine_side_effects.html